Vigabatrin (γ-vinyl-GABA) was developed as a structural γ-aminobutyricacid (GABA) analogue with a vinyl appendage through a systematic search for agents that can increase brain GABA levels through inhibition of GABA transaminase. The onset of anticonvulsant activity of vigabatrin in seizure and epilepsy models, such as audiogenic seizures in mice, occurs with a delay, being correlated with the gradually developing increase in GABA levels in nerve terminals rather than with the concentration of the drug in plasma. It is highly effective and relatively well tolerated in the treatment of infantile spasms. Vigabatrin is a first-line drug for the treatment of infantile spasms, particularly those caused by tuberous sclerosis complex. Because of the risk of irreversible visual field constriction, vigabatrin is rarely used in other indications. The first oscillatory potential and 30-Hz flicker responses of the ERG seem to be correlated with vigabatrin-associated visual field defects.